Evidence map›Paper›PMID 22011235›Full record

ReviewCritical reviews in biomedical engineering2011

Role of airway recruitment and derecruitment in lung injury.

Samir Ghadiali, Y Huang

Abstract readReview
In one paragraph

Review in Critical reviews in biomedical engineering, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Mechanical ventilation energy analysis: Recruitment focuses injurious power in the ventilated lung.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The POOR Get POORer: A Hypothesis for the Pathogenesis of Ventilator-induced Lung Injury.American journal of respiratory and critical care medicine · 2020
    Review
  10. Article
  11. Article
  12. Optimal Ventilator Strategies in Acute Respiratory Distress Syndrome.Seminars in respiratory and critical care medicine · 2019
    Review
  13. Article
  14. Plasma membrane wounding and repair in pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2017
    Review
  15. Article
  16. Article
  17. TRIM72 is required for effective repair of alveolar epithelial cell wounding.American journal of physiology. Lung cellular and molecular physiology · 2014
    Article
  18. The unusual symmetric reopening effect induced by pulmonary surfactant.Journal of applied physiology (Bethesda, Md. : 1985) · 2014
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Samir GhadialiDepartment of Biomedical Engineering, The Ohio State University, Columbus, Ohio 43221, USA. ghadiali.1@osu.edu
Y Huang
The Ohio State University · US

Funding

Biomechanical Evaluation of Eustachian Tube DysfunctionR01DC007230 · NIDCD · OHIO STATE UNIVERSITY · PI GHADIALI, SAMIR N · 2006 to 2010
$704k
NIDCD NIH HHS R01 DC007230
6 · The paper itself

Abstract

The mechanical forces generated during the ventilation of patients with acute lung injury causes significant lung damage and inflammation. Low-volume ventilation protocols are commonly used to prevent stretch-related injury that occurs at high lung volumes. However, the cyclic closure and reopening of pulmonary airways at low lung volumes, i.e., derecruitment and recruitment, also causes significant lung damage and inflammation. In this review, we provide an overview of how biomedical engineering techniques are being used to elucidate the complex physiological and biomechanical mechanisms responsible for cellular injury during recruitment/derecruitment. We focus on the development of multiscale, multiphysics computational models of cell deformation and injury during airway reopening. These models, and the corresponding in vitro experiments, have been used to both elucidate the basic mechanisms responsible for recruitment/derecruitment injury and to develop alternative therapies that make the epithelium more resistant to injury. For example, models and experiments indicate that fluidization of the cytoskeleton is cytoprotective and that changes in cytoskeletal structure and cell mechanics can be used to mitigate the mechanotransduction of oscillatory pressure into inflammatory signaling. The continued application of biomedical engineering techniques to the problem of recruitment/derecruitment injury may therefore lead to novel and more effective therapies.

Indexed as

AnimalsBiomechanical PhenomenaBiomedical EngineeringComputational BiologyHumansLung ComplianceLung InjuryLung Volume MeasurementsMechanotransduction, CellularRespiration, ArtificialRespiratory Function TestsRespiratory Mechanics

Identifiers

PMID22011235
PMCPMC3205463
OpenAlexW2080791174

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.